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Co‐expression of CD79a (JCB117) and CD3 by lymphoblastic lymphoma
Author(s) -
Pilozzi Emanuela,
Pulford Karen,
Jones Margaret,
MüllerHermelink HansKonrad,
Falini Brunangelo,
Ralfkiaer Elisabeth,
Pileri Stefano,
Pezzella Francesco,
de WolfPeeters Christine,
Arber Daniel,
Stein Harald,
Mason David,
Gatter Kevin
Publication year - 1998
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/(sici)1096-9896(1998100)186:2<140::aid-path149>3.0.co;2-y
Subject(s) - lymphoblastic lymphoma , cd3 , lymphoma , b cell , cancer research , pathology , antibody , t cell , biology , medicine , immunology , antigen , immune system , cd8
Acute lymphoblastic leukaemia/lymphoma is a malignant disorder derived from the clonal proliferation of lymphoid precursor cells. Whether the tumour cells are of B‐ or T‐cell type is an important criterion for prognosis which has not been available previously to pathologists, due to the lack of a reliable early B‐cell marker functioning on routinely processed material. This has changed with the production of monoclonal antibodies against the B‐cell signalling molecule CD79a. CD79a is expressed on normal and neoplastic B cells from the early stages of B‐cell maturation and has been considered to be B‐cell‐specific. Currently available antibodies against CD79a, in particular JCB117, allow the identification of B cells, and hence B lymphoblastic disease, in paraffin‐embedded material. In this study, the expression of CD79a (JCB117) and CD3 has been investigated in 149 cases of T and 68 cases of B lymphoblastic leukaemia/ lymphoma. For the first time, co‐expression of CD79a (JCB117) and CD3 is reported in 10 per cent of cases of T lymphoblastic leukaemia/lymphoma. This finding raises questions about the co‐expression of T‐ and B‐cell markers in the development of lymphocytes, benign as well as malignant, and alerts pathologists to a potential problem in diagnosis. Copyright © 1998 John Wiley & Sons, Ltd.